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Liver Abscess

1. PYOGENIC LIVER ABSCESS

Etiology

  • Abscesses arise in the liver as a result of bacterial infection
  • Potential routes of hepatic exposure to bacteria
    • Biliary tree, portal vein, hepatic artery, direct spread, trauma
  • Most common organisms
    • E.coli, K.pneumoniae, S.aureus, Enterococci, Bacteroides

Pathogenesis

  • Infection from the biliary tree – most common cause
    • Biliary obstruction leads to bile stasis – this creates nidus for bacteria colonisation
    • Infection can then ascend to the liver – ascending suppurative cholangitis
  • Portal vein sepsis
    • Portal vein drains the GIT – so any infection of GIT can cause ascending portal vein infection
    • E.g. Diverticulitis, appendicitis, pancreatitis, inflammatory bowel disease (IBD), pelvic inflammatory disease
  • Systemic infections through hepatic artery
    • Endocarditis, pneumonia, osteomyelitis, bacteraemia
  • Direct extension of a nearby infection
    • Suppurative cholecystitis, subphrenic abscess, perforation
  • Penetrating/blunt trauma – form haematoma and necrosis of liver

Pathology

  • 75% cases involve the right lobe due to preferential laminar blood flow and larger blood supply
  • Abscesses can coalesce to give a honeycomb appearance

Clinical features

  • Right upper quadrant pain, fever
  • Jaundice – in a third of patients
  • Hepatomegaly
  • General malaise, chills
  • Pleural effusion

Investigations

  • Blood – ↑ALP, leukocytosis, ↑ESR
  • CXR – elevated right hemidiaphragm, right sided pleural effusion
  • US – shows round/oval hypoechoic areas
  • CT

Treatment

  • Broad spectrum antibiotics – start empirically until culture is available
    • Should cover gram negative and anaerobic bacteria – 3rd generation cephalosporins, metronidazole, aminoglyosides
  • Percutaneous drainage of abscess under US guidance

2. AMOEBIC LIVER ABSCESS

Epidemiology/Etiology

  • Entamoeba Histolytica – exists as cysts in a vegetative form, capable of surviving outside the human body
  • Prevalent in tropical climates, especially in areas with poor sanitation
  • More common in alcoholic/cirrhotic patients
  • Transmission is via the faecal-oral route

Pathogenesis

  • Cyst is swallowed via food/water that is contaminated with faeces – the cyst is resistant to gastric acid
  • It then enters small intestine undamaged and reaches distal ileum/caecum where the trophozoite is released and multiplies
  • It infects the liver through the inferior mesenteric or portal vein (see pic)
    • Trophozoites destroy hepatocytes by releasing histiolysin – cause amoebic hepatitis and multiple microabscesses
    • It can resolve spontaneously or lead to a localised amoebic liver abscess
    • Abscess is more common in right posterior-superior region of the liver
    • Liquefaction necrosis occurs which forms a thick chocolate brown pus (anchovy sauce)
      • Consists of dead hepatocytes, RBCs, and necrotic material
  • There is risk of rupture and spread

Course of abscess and consequences

  • Rupture into lungs – leads to chocolate coloured sputum
  • Rupture into peritoneum – peritonitis (emergency)
  • Rupture into pleural cavity – empyema
  • Rupture into bronchus – bronchopleural fistula
  • Rupture into skin – amoebiasis cutis
  • Rupture into pericardial cavity – cardiac tamponade (high mortality)
  • Septicaemia in patients with cirrhosis

Clinical features

  • High fever, sweating, weight loss, cough
  • Right upper quadrant pain and tenderness
  • Leukocytosis
  • Right sided pleural effusion
  • Amoebic dysentery

Investigations

  • US, CT – raised diaphragm, abscess cavity, size, location, presence of effusion
  • XR – raised fixed diaphragm, pleural effusion, soft tissue shadow
  • LFTs
  • Aspiration – microscopy
  • PCR

Treatment

  • Metronidazole 750mg t.d.s for 5-10 days
  • IV/oral antibiotics to control secondary infection – cefotaxime, amoxicillin
  • US guided aspiration – in the 9th + 10th intercostal space
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